Up-regulation of a cellular protein at the translational level by a retrovirus.
Up-regulation of a cellular protein at the translational level by a retrovirus.
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逆转录病毒在翻译水平上调细胞蛋白。
DOI：
10.1073/pnas.0710526105
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发表时间：
2008
影响因子：
11.1
通讯作者：
Hudson,AlanP
中科院分区：
文献类型：
--
作者：
Yoshimura,FaythK;Luo,Xixia;Zhao,Xiaoqing;Gerard,HerveC;Hudson,AlanP
貂细胞灶形成（MCF）小鼠白血病病毒（MLV）是小鼠胸腺淋巴瘤的病原体。我们以前已经观察到，某些类型的细胞，如白血病前胸腺淋巴细胞和培养的水貂上皮细胞的MCF 13 MLV的重叠感染，导致病毒包膜前体多聚蛋白的积累，导致内质网（ER）应激的诱导。在这项研究中，我们证明了MCF 13 MLV感染诱导的ER应激导致真核起始因子2 α亚基磷酸化的增加。在发生这种情况的细胞中，我们已经检测到细胞凋亡蛋白1（c-IAP 1）的细胞抑制剂的上调。实时RT-PCR定量的信息水平和蛋白质周转试验的结果表明，上调的c-IAP 1发生在翻译水平。在MCF 13 MLV诱导的胸腺淋巴瘤和慢性感染的水貂上皮细胞中，可检测到转录后步骤的c-IAP 1水平升高。简单的逆转录病毒在翻译水平上调节细胞基因表达的能力可能是导致发病的重要机制。
Mink cell focus-forming (MCF) murine leukemia viruses (MLVs) are the etiologic agent of thymic lymphoma in mice. We have observed previously that superinfection by MCF13 MLV of certain cell types, such as preleukemic thymic lymphocytes and cultured mink epithelial cells, results in the accumulation of the viral envelope precursor polyprotein, leading to the induction of endoplasmic reticulum (ER) stress. In this study, we demonstrate that the induction of ER stress by MCF13 MLV infection results in an increase in the phosphorylation of the α-subunit of eukaryotic initiation factor 2. In cells in which this occurs, we have detected an up-regulation of the cellular inhibitor of apoptosis protein 1 (c-IAP1). The results of real-time RT-PCR quantification of message levels and protein turnover assays indicate that up-regulation of c-IAP1 occurs at the translational level. Elevation of c-IAP1 levels at a posttranscriptional step was detectable in MCF13 MLV-induced thymic lymphomas and chronically infected mink epithelial cells. The ability of a simple retrovirus to regulate cellular gene expression at the translational level may be an important mechanism that contributes to pathogenesis.